China
Africa
Explore chapters and articles related to this topic
Cerebral Biopsy in the Neurochemical Study of Alzheimer Disease
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
Andrew W. Procter, David M. Bowen
Although cortical tissue from patients with deep-seated neoplastic lesions seems suitable as a control group, the use of such material has been questioned (Tarbit et al, 1981; Sherwin et al, 1988). Therefore in a recent study (Lowe et al, 1989) two additional groups were used and the content of free amino acids determined. Of the abundant ones, aspartate, glutamine and serine, showed significant differences in concentration between subgroups of the non- demented subjects. Values for the other compounds in neocortex removed for access to deep-seated neoplastic lesions were taken as an indication of values for normal tissue. Content of the other abundant amino acids were in AD, either unaltered (GABA, glycine and taurine), increased (alanine), or decreased (glutamate). Content of the latter for individual AD samples from the mid-temporal gyrus shows a correlation with pyramidal neurone count in cortical layer III.
Animal models of vascular dementia with emphasis on stroke-prone spontaneously hypertensive rats
Published in H. Saito, Y. Yamori, M. Minami, S.H. Parvez, New Advances in SHR Research –, 2020
Hideya Saito, Hiroko Togashi, Mitsuhiro Yoshioka, Nishio Nakamura, Masaru Minami, Hasan S. Parvez
The SHRSP brain was compared to a brain obtained from the autopsy of a patient with multiple cerebral infarction to determine whether or not similar pathological changes occurred. In the cerebral cortex of both the human case and the SHRSP, there was enlargement of the perivascular space and rarefaction of the parenchyma (Fig. 11) with scattered neuronal loss and astrocytic proliferation. In the SHRSP cerebral cortex, the population of neurons as well as the width of the cortical layer was smaller than in the human brain. However, this feature of neuronal depopulation in the SHRSP cerebral cortex was very similar to that seen in the human case (Fig. 10). In white matter, focal cystic changes with proliferation of macrophages and reactive astrocytes were observed (Fig. 12).
EEG changes between sleeping and wakefulness
Published in Philip N. Murphy, The Routledge International Handbook of Psychobiology, 2018
Julia K. M. Chan, Christian L. Nicholas
The delta oscillations characteristic of SWS are thought to be generated at two levels of the central nervous system (CNS, Amzica & Steriade, 1998; Amzica & Steriade, 2000; Steriade & Amzica, 1998), in the cerebral cortex (cortical delta) and in the thalamus (thalamic ‘clock-like’ delta). Thalamic delta is thought to be intrinsic to thalamic relay cells and is caused by a combination of two inward flowing depolarising currents. The first is a transient calcium current and the second is a hyperpolarisation activated cation current. The latter comes into play when the thalamic relay cell resting membrane potential falls below -65 mV to -70 mV, due to GABAergic inhibition from thalamic reticular nuclei (Steriade, 1999a, 1999b). When resting membrane potential falls to this point the relay cells switch from a tonic mode of firing, where information is easily transmitted through to the cortex, to a bursting mode, where less peripherally stimulated cortical activation occurs. This intrinsic thalamic oscillation is synchronised by a number of thalamic and supra-thalamic mechanisms. These mainly involve cortico-thalamic feedback to the reticular nucleus (generally from cortical layer IV), intrinsic cortico-cortical connections (cortical layers II and III) and slowly oscillating cortical cells in cortical layers III–VI (Steriade, 1999a; Steriade, Nunez, & Amzica, 1993a, 1993b).
Effects of maternal diazinon exposure on frontal cerebral cortical development in mouse embryo
Published in International Journal of Neuroscience, 2023
Fatemeh Saraei, Seyed Homayoon Sadraie, Gholam Reza Kaka, Mehrangiz Sadoughi, Nayereh Afzal Nejad, Nahid Sarahian
The results of this study showed the weight of the fetuses that mothers were exposed to Diazinon did not increase significantly. Previous studies have shown that pregnant mice in 6th to 15th days of gestation who were exposed to doses of diazinon (up to 100 mg/kg/day) their fetuses gained weight by increasing the dose of diazinon. These findings were consistent with our findings [23]. One study showed that exposure to 0.1–15 ppm Diazinon had no influence on diet and the weight of animals [24]. However, it is difficult to assume a mechanism by which exposure to diazinon before birth can affects fetal weight gain. Our histomorphometric study revealed the mean of total cortical layer thickness was significantly decreased in EXP 2 group in comparison to control and sham groups. However the mean thickness frontal CP of brain in experimental groups compared to the control group was significantly increased.
Thalamic neuromodulation in epilepsy: A primer for emerging circuit-based therapies
Published in Expert Review of Neurotherapeutics, 2023
Bryan Zheng, David D. Liu, Brian B Theyel, Hael Abdulrazeq, Anna R. Kimata, Peter M Lauro, Wael F. Asaad
Because classification schemes based primarily on local anatomy and histology do not capture the functional heterogeneity of individual thalamic nuclei, some modern thalamic classification systems are based on circuit topology[26]. Distinctions have been made based on (i) the characteristics of thalamocortical output – core versus matrix nuclei[27], (ii) input – first- versus higher-order nuclei[28], or (iii) both input and output[29]. For example (of [i]), the anterior nucleus of the thalamus (ANT) has been defined as a core nucleus because it provides focal projections as a node in the medial limbic circuit. The pulvinar nucleus, specifically the PuM, also possesses ‘core-like’ properties based on its distinct circuits involving the temporal lobe[24]. In contrast, matrix nuclei like the centromedian nucleus of the thalamus (CMT) are characterized by markedly more diffuse cortical projections[30]. Meanwhile, within the framework of the first- and higher-order nuclear scheme (ii): first-order nuclei receive ‘driver’ inputs from subcortical sites carrying primary sensory information (e.g. lateral geniculate nucleus [LGN] receives visual input from the retina), while higher-order nuclei (e.g. the pulvinar) receive driver inputs from cortical layer V and primarily participate in transthalamic cortico-cortical circuits[28]. This classification scheme is useful in that it highlights how the thalamus continues to be involved in information processing between areas of cortex in addition to modulating and relaying primary sensory information.
Ocular Manifestations of Neuronal Ceroid Lipofuscinoses
Published in Seminars in Ophthalmology, 2021
Rohan Bir Singh, Prakash Gupta, Akash Kartik, Naba Farooqui, Sachi Singhal, Sukhman Shergill, Kanwar Partap Singh, Aniruddha Agarwal
Mutations in the CLN6 gene coding for a transmembrane ER protein of unknown significance causes CLN-6 disease [earlier known as autosomal recessive, variant-late infantile neuronal ceroid lipofuscinosis (vLINCL)].111 CLN-6 protein is highly expressed in bipolar cells and photoreceptors, and the mutations in the gene leads to production of truncated non-function protein, resulting in degeneration of these cells during different phases of the disease.112 The age of disease onset is highly variable, ranging from 18 months to 8 years, and leads to death in the affected individuals by mid-20s. The clinical presentation includes cognitive and motor regression, progressive cerebellar, pyramidal, and extrapyramidal signs and seizures. It presents with visual failure leading to blindness, with many showing consistently normal fundus findings.106,113 Additionally, CLN6 mutations are known to cause the autosomal recessive variants of Kufs disease, as mentioned previously. The skin biopsy shows cytoplasmic vacuoles containing mixed curvilinear profiles and fingerprint profiles. However, if skin biopsy is negative for storage material, deep rectal or brain biopsies can be considered, especially in adult patients. Neuroimaging shows deep cortical layer-specific neuron loss; and cerebellar atrophy.100 An ongoing clinical trial is assessing the long-term efficacy of AAV based working gene transfer therapy as performed for the treatment CLN-3.114